The widespread use of zinc oxide nanoparticles (ZnO-NPs) and their release into theenvironment have raised concerns about the potential toxicity caused by dietary transfer. However,the toxic effects and the mechanisms of dietary transfer of ZnO-NPs have rarely been investigated.We employed the bacteria-feeding nematode Caenorhabditis elegans as the model organism to inves-tigate the neurotoxicity induced by exposure to ZnO-NPs via trophic transfer. Our results showedthat ZnO-NPs accumulated in the intestine of C. elegans and also in Escherichia coli OP50 that theyingested. Additionally, impairment of locomotive behaviors, including decreased body bendingand head thrashing frequencies, were observed in C. elegans that were fed E. coli pre-treated with ZnO-NPs, which might have occurred because of damage to the D-type GABAergic motor neurons.However, these toxic effects were not apparent in C. elegans that were fed E. coli pre-treated withzinc chloride (ZnCl2). Therefore, ZnO-NPs particulates, rather than released Zn ions, damage theD-type GABAergic motor neurons and adversely affect the locomotive behaviors of C. elegans viadietary transfer.
